Výsledky vyhledávání - "A. Andrea Gudiel"

Akademický článek

Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 signaling

Autor: David M. Walter, Amy C. Gladstein, Katherine R. Doerig, Ramakrishnan Natesan, Saravana G. Baskaran, A. Andrea Gudiel, Keren M. Adler, Jonuelle O. Acosta, Douglas C. Wallace, Irfan A. Asangani, David M. Feldser

Publikováno v: Communications Biology, Vol 6, Iss 1, Pp 1-11 (2023)

SETD2 inactivation leads to heightened mTORC1 signaling, oxidative metabolism and protein synthesis in KRAS-driven mouse models of lung adenocarcinoma, contributing to the understanding of how SETD2 deficiency drives early and widespread tumor growth

Externí odkaz: https://doaj.org/article/c2c79fc965134987aff07bf0f609c365

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Akademický článek

Context-Dependent Effects of Amplified MAPK Signaling during Lung Adenocarcinoma Initiation and Progression

Autor: Michelle Cicchini, Elizabeth L. Buza, Kyra M. Sagal, A. Andrea Gudiel, Amy C. Durham, David M. Feldser

Publikováno v: Cell Reports, Vol 18, Iss 8, Pp 1958-1969 (2017)

Expression of oncogenic KrasG12D initiates lung adenomas in a mitogen-activated protein kinase (MAPK) signal-dependent manner from only a subset of cell types in the adult mouse lung. Amplification of MAPK signaling is associated with progression to

Externí odkaz: https://doaj.org/article/18253b216cca47dc9a2732008fcf0a29

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Supplementary Table 3 from Systematic In Vivo Inactivation of Chromatin-Regulating Enzymes Identifies Setd2 as a Potent Tumor Suppressor in Lung Adenocarcinoma

Autor: David M. Feldser, Travis J. Yates, Michelle Cicchini, Caroline Kim-Kiselak, A. Andrea Gudiel, Charuhas Deshpande, John W. Tobias, Elizabeth L. Buza, Olivia S. Venancio, David M. Walter

Supplementary Table 3: Gene ontology analysis for genes deregulated by both Arid1a and Setd2 loss.

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5c4fe00ed8f0169ad9244e103bd52315
https://doi.org/10.1158/0008-5472.22416824.v1

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Supplementary Figure Legends from Systematic In Vivo Inactivation of Chromatin-Regulating Enzymes Identifies Setd2 as a Potent Tumor Suppressor in Lung Adenocarcinoma

Autor: David M. Feldser, Travis J. Yates, Michelle Cicchini, Caroline Kim-Kiselak, A. Andrea Gudiel, Charuhas Deshpande, John W. Tobias, Elizabeth L. Buza, Olivia S. Venancio, David M. Walter

Figure legends for supplementary figures.

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0522efbac8f25153fd945a5558707410
https://doi.org/10.1158/0008-5472.22416839

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Data from Systematic In Vivo Inactivation of Chromatin-Regulating Enzymes Identifies Setd2 as a Potent Tumor Suppressor in Lung Adenocarcinoma

Autor: David M. Feldser, Travis J. Yates, Michelle Cicchini, Caroline Kim-Kiselak, A. Andrea Gudiel, Charuhas Deshpande, John W. Tobias, Elizabeth L. Buza, Olivia S. Venancio, David M. Walter

Chromatin-modifying genes are frequently mutated in human lung adenocarcinoma, but the functional impact of these mutations on disease initiation and progression is not well understood. Using a CRISPR-based approach, we systematically inactivated thr

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0c4d8f9067a4b248f9769fb74e9a87ec
https://doi.org/10.1158/0008-5472.c.6509660.v1

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Supplementary Table 2 from Systematic In Vivo Inactivation of Chromatin-Regulating Enzymes Identifies Setd2 as a Potent Tumor Suppressor in Lung Adenocarcinoma

Autor: David M. Feldser, Travis J. Yates, Michelle Cicchini, Caroline Kim-Kiselak, A. Andrea Gudiel, Charuhas Deshpande, John W. Tobias, Elizabeth L. Buza, Olivia S. Venancio, David M. Walter

Supplementary Table 2: Ingenuity Pathway Analysis results for Setd2 vs. GFP tumors.

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::71edf1c1a536f37d85b263f5b21f1fcc
https://doi.org/10.1158/0008-5472.22416827.v1

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Supplementary Table 1 from Systematic In Vivo Inactivation of Chromatin-Regulating Enzymes Identifies Setd2 as a Potent Tumor Suppressor in Lung Adenocarcinoma

Autor: David M. Feldser, Travis J. Yates, Michelle Cicchini, Caroline Kim-Kiselak, A. Andrea Gudiel, Charuhas Deshpande, John W. Tobias, Elizabeth L. Buza, Olivia S. Venancio, David M. Walter

Supplementary Table 1: Ingenuity Pathway Analysis results for Arid1a vs. GFP tumors.

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8411fa203e34ae600e0c242c6c865877
https://doi.org/10.1158/0008-5472.22416830

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Supplementary Figures 1-10. from Systematic In Vivo Inactivation of Chromatin-Regulating Enzymes Identifies Setd2 as a Potent Tumor Suppressor in Lung Adenocarcinoma

Autor: David M. Feldser, Travis J. Yates, Michelle Cicchini, Caroline Kim-Kiselak, A. Andrea Gudiel, Charuhas Deshpande, John W. Tobias, Elizabeth L. Buza, Olivia S. Venancio, David M. Walter

Supplementary Figure 1: Locations and types of chromatin regulator mutations found in human lung adenocarcinomas. Supplementary Figure 2: Identification of high efficiency Brg1, Arid1a and Setd2 sgRNAs using a fluorescent reporter-based sensor assay.

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::573043a7e6ec9f454775db49cc43eeb6
https://doi.org/10.1158/0008-5472.22416833

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Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 signaling

SETD2 is a tumor suppressor that is frequently inactivated in several cancer types. The mechanisms through which SETD2 inactivation promotes cancer are unclear, and whether targetable vulnerabilities exist in these tumors is unknown. Here we identify

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::72a47993f898eae9c514211d3a1bbcb6
https://doi.org/10.1101/2022.10.06.511146

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Copper is an essential regulator of the autophagic kinases ULK1/2 to drive lung adenocarcinoma

Autor: Donita C. Brady, Tiffany Tsang, Jessica M. Posimo, Michelle Cicchini, David M. Feldser, A. Andrea Gudiel

Publikováno v: Cell Stress
Nature cell biology

Targeting aberrant kinase activity in cancer relies on unmasking cellular inputs such as growth factors, nutrients, and metabolites that contribute to cancer initiation and progression1. While the transition metal copper (Cu) is an essential nutrient

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d1e83bab08c0e6fabc11402c6e353a4b
https://doi.org/10.1038/s41556-020-0481-4

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